2023.7.18: bk.psy/schiz/Amber Needham 2022`The Blind Girl Sees:
Amber Needham 2022`The Blind Girl Sees
5-star/informative and inspiring:
any noteworthy thing not relevant to Americium Dream Documents .
2023.7.18: bk.psy/schiz/Amber Needham 2022`The Blind Girl Sees:
Amber Needham 2022`The Blind Girl Sees
5-star/informative and inspiring:
2023.3.2: web.health/diet/aspirin/blindness/
low-dose aspirin seems good for eyes except with vitamins:
summary:
. there are some studies that seemed to show
that aspirin increased your risk of blindness;
but the best type of study (randomized trials)
showed they actually reduced the risk of blindness
unless you happen to be the user of multivitamins.
. one study showed that only people with good genes
may benefit from a good diet;
but you should be safe from AMD blindness if you
limit both omega-6 vegetable oils and your glycemic load.
https://scholar.google.com/scholar?hl=en&as_sdt=0%2C3&q=omega-6+%2C+amd+blindness
Ophthalmology. 2019
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6875604/
The association of aspirin use with
age-related macular degeneration progression
in the Age-Related Eye Disease Studies: AREDS2 Report No. 20.
. there are 2 randomized clinical trials:
Arch Ophthalmol. 2001:
Age-related maculopathy in a randomized trial of low-dose aspirin among US physicians.
Ophthalmology. 2009:
Low-dose aspirin and medical record-confirmed age-related macular degeneration in a randomized trial of women.
. using 100mg aspirin every other day
slightly reduced your risk of AMD
yet increased your risk if you used certain multivitamin supplements.
"Among current nonusers of multivitamins,
those in the aspirin group had a statistically-significant
32% reduced risk of AMD (HR, 0.68; 95% CI, 0.49−0.95)
whereas among current users of multivitamins,
there was a nonsignificant 14% increased risk of AMD
in the aspirin group (HR, 1.14; 95% CI, 0.76−1.70)"
[ Ophthalmology. 2009
https://pubmed.ncbi.nlm.nih.gov/19815293/
Low-Dose Aspirin and Medical Record Confirmed
Age-related Macular Degeneration in a Randomized Trial of Women;
William G. Christen, Sc.D, et al.]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2787838/
"men assigned to alternate-day low-dose aspirin (325 mg)
had a statistically non-significant
22% reduced risk of visually-significant AMD
during a five year treatment period."
. placebo terminated early due to aspirin causing
a 44% reduced risk of first myocardial infarction.
[ Arch Ophthalmol. 2001
https://pubmed.ncbi.nlm.nih.gov/11483080/
Age-related maculopathy in a randomized trial of
low-dose aspirin among US physicians;
W G Christen et al.]
"In AREDS, both aMedi[Mediterranean-type diet] and its fish component
interacted with CFH rs10922109 for late AMD
(P = 0.01 and P = 0.0005, respectively);
higher aMedi and fish intake were each associated with
decreased risk of AMD only in participants with protective alleles.
Closer adherence to a Mediterranean-type diet
was associated with lower risk of progression to late AMD and to large drusen.
The signal was greater for GA than neovascular AMD.
Fish intake contributed to this protective association.
CFH genotype strongly influenced these relationships.
Hazard ratios (HRs) for progression in aMedi tertile 3 versus 1
were 0.78 (95% confidence interval [CI], 0.71-0.85, P < 0.0001)
for late AMD, 0.71 (0.63-0.80, P < 0.0001) for GA,
and 0.84 (0.75-0.95, P = 0.005) for neovascular AMD.
For fish consumption, HRs for late AMD in quartile 4 versus 1 were
0.69 (0.58-0.82, P < 0.0001; AREDS) and
0.92 (0.78-1.07, P = 0.28; AREDS2).
. the HR for progression to large drusen in aMedi tertile 3 versus 1 was
0.79 (0.68-0.93, P = 0.004)."
[ Ophthalmology. 2020
https://pubmed.ncbi.nlm.nih.gov/32348832/
Adherence to the Mediterranean Diet and Progression to
Late Age-Related Macular Degeneration
in the Age-Related Eye Disease Studies 1 and 2;
TiarnĂ¡n D Keenan, et al;
Age-Related Eye Disease Studies (AREDS) 1 and 2 Research Groups.]
Dr. Barry Sears 2002`The Omega Rx Zone:[ad]
The Miracle of the New High-Dose Fish Oil
The Mediterranean Zone: [ad]
Unleash the Power of the World's Healthiest Diet for Superior Weight Loss, Health, and Longevity Hardcover – 2014 by Dr. Barry Sears (Author)
2023.1.22: news.health/diet/blindness/amd/metformin:
. if your blood sugar is borderline high,
then you might be a candidate for taking metformin;
that drug is now known to reduce the risk of blindness
by inhibiting retina death (geographic atrophy)
and by inhibiting intraocular neovascularization (wet AMD).
Int J Ophthalmol. 2021 Aug:
https://pubmed.ncbi.nlm.nih.gov/34414094/
Newly-found functions of metformin
for the prevention and treatment of age-related macular degeneration;
Kuan-Rong Dang, Tong Wu, Yan-Nian Hui, Hong-Jun Du.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8342286/
22.6.6: web.health/diet/blindness/amd/
lowering vegf helps amd? several herbs lower vegf:
summary:
. several methods of cancer treatment
are anti-angiogenic: they work by
stopping new blood vessel growth.
. one thing that cancers and amd blindness
have in common, is excess production of vegf
(vascular endothelial growth factor)
that causes the rapid growth of blood vessels
that tend to be leaky and result in edema.
. for wet amd (age-related macular degeneration
with high vegf that results in leaks and edema)
the only anti-vegf treatments have been injections
that are very expensive and can be painful.
. several herb are known to lower vegf,
and I wondered if taking them orally
could lower vegf in the eye.
2022.5.23: health/diet/egg/blindness/
more orange yolk means less AMD blindness:
summary:
. a yolk that is more orange (than yellow)
is likely to have more lutein and zeaxanthin
that reduces the risk of AMD blindness.
. organic eggs have rules about
the coloring additives added to chicken feed.
. if you are not certain about the quality
of the coloring in your egg,
you can supplement with zeaxanthin and lutein.
[eg, MacuGuard® Ocular Support with Saffron:
https://www.lifeextension.com/vitamins-supplements/item01992/macuguard-ocular-support-with-saffron
10 mg free lutein,
4 mg meso-zeaxanthin & trans-zeaxanthin.]
. taking the supplement with yolk
might increase its bioavailability
because MacuGuard claims to use Phospholipids
in order to enhance lutein absorption,
and egg yolk contains Phospholipids.
[ Nutrients. 2015
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4425170/
Egg Phospholipids and Cardiovascular Health.
Christopher N. Blesso]
2022.3.9: health/diet/omega-6/
chronic illness increased after oils of soy, grain, and seeds added to diet:
Dr. Chris Knobbe warns us that we are wrong about
omega-6 oil being healthy at higher doses.
AncestryFoundation 2021
https://www.youtube.com/watch?v=sKR1ZdHXXzo
Omega-6 Apocalypse 2 (AHS21)
Catherine Shanahan M.D. 2018: [ad]
http://www.amazon.com/dp/B01G1J7WEU/ref=nosim?tag=americiu-20
Deep Nutrition: Why Your Genes Need Traditional Food.
The origin of Eagle Eyes® began at. here are the wrap-arounds of various shades .
NASA's Jet Propulsion Laboratory
to protect eyesight from solar radiation light.
. eagles have unique oil droplets in their eyes
that selectively filter out harmful radiation
and permit only specific wavelengths of light;
NASA replicated this into a lens technology
that, in turn, resulted in Eagle Eyes® eyewear.
"Metformin's strong anti-inflammatory properties
by activating an enzyme called AMPK,
which in turn damps down
the activity of the protein NF-kappa B.
The inhibition of that suppresses the production of
inflammatory signaling molecules
-- cytokines and chemokines --
needed to initiate and sustain uveitis.
Uveitis causes 10 to 15 % of all blindness in the USA
and even higher proportions of blindness globally.
The only conventional treatment is steroid therapy,
which has serious side effects and cannot be used long-term.
. this study indicates that diet
plays a considerable role in
the risk of [needing and being eligible for]
cataract extraction
in at least a certain Italian population,
with a protective action played by
some vegetables, fruit, calcium, folic acid,and vitamin E,
and an increased risk
associated with elevated salt and fat intake [6.29:
-- this could have been a measure of
where these Italians were getting their
extra doses of salt and fat:
the usual culprit is luncheon meat
-- known to promote diabetes by
mixing sugar with the meat .]
. a significant inverse trend in risk,
were found for intake of
meat (OR 0.6, 95% CI 0.4 to 0.9),
cheese (OR 0.7, 95% CI 0.5 to 1.0),
[implied a more low-carb' diet?
the atkins effect .
6.19: ie,
not necessarily an endorsement
of cheese ! ]
cruciferae (OR 0.5, 95% CI 0.3 to 0.8),
spinach (OR 0.6, 95% CI 0.4 to 0.9),
tomatoes (OR 0.5, 95% CI 0.4 to 0.8),
peppers (OR 0.7, 95% CI 0.4 to 1.1),
citrus fruit (OR 0.5, 95% CI 0.2 to 1.3),
and melon (OR 0.5, 95% CI 0.4 to 0.8).
. a significant increase in risk
was found for
the highest intake of
(compared to the lowest intake)
butter (OR 2.8, 95% CI 1.2 to 6.4),
[6.29: apparently Italian cheese is
not a significant source of butter ? ]
total fat(OR 1.8, 95% CI 1.2 to 2.8),
[ie, sat'fats vs oils]
salt (OR 2.4, 95% CI 1.4 to 4.0)
[luncheon meats vs fresh meats]
. a significant increase in risk
was found for consumption of
oil other than olive oil
[mono'fats vs poly'fats]
(OR 1.6, 95% CI 1.1 to 2.2).
Among micronutrients,
lower ORs for cataract extraction
(highest quintile of intake compared to the lowest)
were found for intake of
calcium (OR 0.5, 95% CI 0.3 to 0.8),
folic acid (OR 0.4, 95% CI 0.2 to 0.7),
and vitamin E (OR 0.5, 95% CI 0.3 to 1.0),
[this may have more to do with
the foods that provided these micronutrients]
. intakes of
methionine, retinol, beta-carotene,
and vitamins A, C, and D
were not associated with cataract risk .
. most of the dark green leafy vegetables,[6.20:
have 15-47% of their carotenoids as lutein,
but very little zeaxanthin (0-3%)
while most of the absorbed carotenoid[6.21:
is carried in LDL,
53% of the (lutein, zeaxanthins) group
is carried by HDL .
. melatonin stimulates glutathione production;[6.21:
it is a potent inhibitor of cataracts;
proven in animal models .
Melatonin production slows after age 40,
but by age 60 virtually no melatonin is produced
at a time when most cataracts develop.
. 3 mg of mel at bedtime in elders with AMD
prevented further vision loss (Yi 2005).
. ala prevents cataract by[. the Vitamin Book said vit'E's job was
protecting glutathione synthesis.
. in animal models it reduced cataract by 40%
and protected the lens from losing
vitamins C, E, and glutathione.
. vitamin C is a first-line neutralizer of radical;
it is then recycled by glutathione .
. Selenium works with alpha-lipoic acid
to increase cellular concentrations of glutathione,
. Low plasma levels of vitamin E
increase the risk of lens opacities.
. cysteine is a component of glutathione;50 .. 150 mg riboflavin:
A combination of diallyl disulfide
(a major organosulfide in garlic oil)
and N-acetyl-cysteine (NAC)
completely prevented cataract development in animals.
Riboflavin reduces oxidized glutathione;250 mg Inositol nicotinate:
it is a precursor FADH
(reduced flavin adenine dinucleotide)
which is used by glutathione reductase,
to reduce and activate glutathione;
it makes glutathione available for the enzyme
glutathione-selenium peroxidase,
which neutralizes peroxide free radicals .
. occurs in high concentrations in the lens.2.5 mg folic acid
Inositol quenches reactive oxygen .
. B-6 prevents free-radicals by100-200 mg CoQ10;
properly metabolizing homocysteine
and is required for absorption of vitamin B12,
and proper synthesis of nucleic acids.
. . low levels of the B vitamins that are
critical to the metabolism of homocysteine),
will result in elevated levels of homocysteine,
which is a risk factor for both AMD and
other cardiovascular diseases .
. supplementing with folic acid, B6, and B12
can significantly reduce the risk of AMD
in adults with high homocysteine (Christen 2009).
. Mitochondrial dysfunction can result inDHEA
reactive oxygen species
linked to both cataracts
and macular degeneration;
a combination of CoQ10, acetyl-L-carnitine,
and proper diet,
improved mitochondrial function .
Acetyl-L-carnitine can reduce cataract risk
by acetylating potential glycation sites
that would otherwise cloud lens crystallins .
. abnormally low in patients with AMD (Bucolo 2005).[6.21:
DHEA also has been shown to protect the eyes against
oxidative damage (Tamer 2007).
Gingko biloba has anti-cataract potential;500-1000 mg carnosine
Bilberry, a proanthocyanidin,
Gingko biloba and bilberry may restore
microcapillary circulation.
. bilberry contains Anthocyanidins
and Cyanidin-3-Glucoside (C3G);
. anthocyanidins may prevent leakage from capillaries,
prevalent in neovascular AMD.
Studies also show that bilberry increases
oxidative stress defense mechanisms in the eyes (Milbury 2007).
C3G fights inflammation by
inhibiting inducible nitric oxide synthase (iNOS),
C3G increases cytokine adiponectin
[. helps burn energy instead of letting it
raise sugar levels and increase fat .]
C3G may be protect against Alzheimer’s
[. that wouldn't be surprising,
if it does reduce sugar spiking .]
C3G helps to induce apoptosis
in a number of human cancer lines .
Bioflavonoids are powerful inhibitors of
the enzyme aldose reductase.
If aldose reductase activity falls,
sorbitol is not synthesized.
This reduces the accumulation of
water in the lens.
The bioflavonoids quercetin, myrcetin,
and kaempferol (from limes)
specifically inhibit diabetic cataracts.
Gingko is a widely used flavonoid that
maintains microcirculation to the eye
and inhibits free radicals.
inhibits formation of AGEsEye drops containing N-acetyl-L-carnosine
(advanced glycation end products)
can delay vision senescence in humans:Phil Micans PharmB, Vice President, IAS Group:
effective in 100% of primary senile cataract cases
and 80% of mature senile cataract cases.
N-acetyl-L-carnosine eye drops are approved for
human use in Russia for the treatment of many eye diseases.
Brite Eyes II contains
1% N-acetyl-L-carnosine
L-Carnosine is an anti-glycation agent;
Topically applied N-acetyl-carnosine
prevented light-induced DNA strand breaks
and repaired damaged DNA strands (Specht 2000),
and has improved visual acuity,
glare and lens opacification
in animals and humans with advanced cataracts
(Williams 2006, Babizhayez 2009).
. the application of L-carnosine for the treatment ofupdate understanding of cataract:
human cataracts is misleading.
This is because L-carnosine readily becomes a substrate for
the activity of natural peptidases (i.e. carnosinase)
in the aqueous humor.
So much so, that there is
no sign of L-carnosine in the aqueous humor
within 15 minutes after instillation.
Furthermore,
I consider that L-carnosine eye-drops
may even be harmful for eyes because
it gradually releases histamine,
which, located as it would be
in the presence of the eye-lens
is a very toxic agent.
However, NAC eye-drops are resistant to
hydrolysis with natural carnosinase.
Therefore, NAC is the only currently known agent
which reverses and prevents human cataracts.
"The antioxidant activity of L-carnosine (beta-alanyl-L-histidine,wrote M.A. Babizhayev and colleagues.
bioactivated in ocular tissues)
versus N-acetylcarnosine (N-acetyl-beta-alanyl-L-histidine,
ocular-targeted small dipeptide molecules)
was studied in aqueous solution
and in a lipid environment,
employing liposomes as a model of lipid membranes.
Reactive oxygen species (ROS) were generated by an
iron/ascorbate promoter system for induction of lipid peroxidation (LPO),"
investigators in Russia report .
"L-carnosine, which is stabilized from enzymatic hydrolysis,
operates as a universal aldehyde and ROS scavenger
in both aqueous and lipid environments
and is effective at preventing ROS-induced damage
to biomolecules.
Second-generation carnosine analogs bearing the
histidyl-hydrazide moiety
were synthesized and tested versus L-camosine
for their ability to reverse the glycation process,
also known as the Maillard reaction,
and reverse the stable intermolecular cross-links,
monitored in the glucose-ethylamine Schiff base model,
ultimately resulting in the formation of
the advanced glycation end products (AGES)
from nonenzymatic glycation,
accumulating in numerous body tissues and fluids.
The obtained data demonstrate the transglycation properties
of the ophthalmically stabilized L-camosine
and L-carnosine histidyl-hydrazide derivatives tested
and can be used to decrease or predict the occurrence of
long-term complications of AGE formation
and improve therapeutically the quality of vision
and length of life for diabetes mellitus patients
and survivors with early aging.
Scientists at Innovative Vision Products, Inc. (IVP),
developed lubricant eyedrops designed as a
sustained-release 1% N-acetylcarnosine prodrug of L-camosine.
The eyedrops contain a mucoadhesive cellulose-based compound
combined with corneal absorption promoters
and glycerine in a drug-delivery system.
Anti-aging therapeutics with the
eyedrop formula including N-acetylcarnosine
showed efficacy in the nonsurgical treatment of
age-related cataracts for enrolled participants
in the prospective, randomized, double-masked,
placebo-controlled crossover clinical trial
after controlling for age, gender, and daily activities.
In a cohort in excess of 50,500 various patients
seeking cutting-edge medical care,
the N-acetylcamosine topical eyedrops target therapy
was demonstrated to have significant efficacy, safety,
and good tolerability for the prevention and treatment of
visual impairment in this older population
with relatively stable patterns of causes
for blindness and visual impairment.
Overall, accumulated study data demonstrate that
the IVP-designed new vision-saving drugs,
including N-acetylcarnosine eyedrops,
promote health vision and prevent vision disability from
senile cataracts, primary open-angle glaucoma,
age-related macular degeneration, diabetic retinopathy,
and aging.
N-acetylcarnosine eyedrop therapy is the crown jewel of the
anti-aging medical movement
and revolutionizes early detection, treatment,
and rejuvenation of aging-related eye-disabling disorders,"
Epidemiological reviews have suggestedref# Exposure to phenothiazine drugs and risk of cataract.
a possible link between cataract occurrence
and other psychotropic medications,
including benzodiazepines .
. long-term use of corticosteroids, phenothiazines,
certain other antipsychotic drugs,
some antineoplastic agents, and amiodarone
may increase cataract incidence.
. in the mid-1960s,
a decade after the marketing of phenothiazines,
drug-related ocular changes were reported in
patients who had been receiving years of
high-dose antipsychotic medication;
chlorpromazine was the primary offender.
Research also associated cataract occurrence with
other phenothiazines;
thioridazine, thiothixene,
trifluoperazine, levomepromazine,
and perphenazine are frequently cited examples.
A 1999 study of cataract occurrence
compared schizophrenic patients (26%)
with the general population (<1%).
. in addition to pharmaceutical exposures
schiz'ics often have additional risk factors:
smoking and poor dietary habits,
along with emotion-based metabolic disorders
(high cortisol, high insulin,
and blood sugar instabilities) .
[6.21:
. some of the new atypicals are clearly
increasing carb' intolerance,
and thus any cataracts blamed on sugar instabilities
must again point the blame at these meds .]
Epidemiological reviews have suggested
a possible link between cataract occurrence
and other psychotropic medications,
including benzodiazepines
and certain antidepressants
of the tricyclic and mao inhibitor classes .
Clinical reports have indicated an increased risk ofref# Sunlight and other risk factors for cataracts:
ocular opacities in users of phenothiazine drugs,
and some recent epidemiologic studies have found
an association between cataract and a
history of tranquilizer use.
To examine the effects of major tranquilizers
(phenothiazines and haloperidol)
on the risk of cataract extraction,
while controlling for suspected risk factors
such as diabetes and steroid use,
a matched cohort study was performed .
The use of either antipsychotic
or other phenothiazine drugs
increased the risk of cataract extraction
by roughly 3.5 times
in those who were both current users
and were exposed some time in the
2 to 5 years prior to their extraction.
Risk was also increased in individuals with
prior use of
antidiabetic agents,
systemic steroids,
and benzodiazepines.
. relation between individual exposure to sunlightrenewed interest in issue with anti-aggressives
and the risk of cataracts.
Sunlight exposure was very slightly related to
all types of opacities combined.
Although the numbers of cases with
each type of opacity was small,
the risk of cataracts was slightly increased
in medium and high exposure categories
for persons having cortical or
posterior subcapsular opacities only,
but not nuclear sclerotic changes.
Persons with dark brown or hazel eyes
are at increased risk.
An unexpected finding was that
persons who reported using tranquilizers
for six months were at increased risk.
. recent questions about quetiapine (seroquel)-- agingeye.net's summary:
as a possible cataract inducer
have increased the current interest in this issue
across the antipsychotic pharmacotherapy spectrum.
. photosensitizing agents
like chlorpromazine and its metabolites
denature proteins,
which become opacified when exposed to sunlight
and are deposited in the lens, cornea, and skin.
Melanin is also considered a probable cause
of lens discoloration
because it traps free radicals produced by
chlorpromazine.
Melanin and chlorpromazine
have a strong bonding affinity.
When chlorpromazine interacts with
ultraviolet-B light,
it produces purple or bluish colored
free-radical metabolites.
This phototoxic reaction creates the
cataract cellular changes.
has also been reported to induce[6.29:
lenticular changes unrelated to pigmentary retinopathy.
[Siddall J:
Ocular complications related to phenothiazines.
Dis Nerv Syst 1968; 29:10-13]
However, contrary reports have indicated
no evidence of lens opacity
in patients taking this drug.
[Barnes G, Cameron M:
Skin and eye changes with chlorpromazine therapy.
Med J Aust 1966; 1:478-481]
the risk of cataract occurrence remains unclear.
Cataract occurrence was observed as an infrequent finding6.22:
during screening for adverse events
before ziprasidone was approved for clinical use.
[Geodon, in Physicians' Desk Reference, 56th ed.
Montvale, NJ, Medical Economics Co, 2002, pp 2688-2692]
However, there is no known causal connection
between this drug and lenticular opacities.
. cataracts from chlorpromazine, thioridazine, and perphenazineHandbook of Psychiatric Drug Therapy
seem to be more frequent in young schiz'ic's
with rates in 22 ... 26%;
the young schiz'ics have an 82%
overall ocular pathology rate .
. these numbers seemed consistent with
smoking and diabetic effects
and there are multiple sources of diabetes
in most schiz'ics:
chronic stress, poor sleep, and bad diet .
. thioridazine > 800 mg results in
irreversible retinal pigmentation
which can result in blindness .
. any anticholinergic may precipitate[trazodone is weakly anticholinergic
narrow-angle glaucoma;
this happens less with the higher-potency 1st gen's,
and by avoiding co.use of antiparkinson drugs,
most of which are anticholinergics
(another class of antiparkinson drugs
is the dopamine releaser, eg: amantadine).
. thioridazine has potent anticholinergic effects .
. the antipsychotics best known for
not causing weight gain (abilify, geodon)
also may cause insomnia that leads to
co.use of benzodiazepines or trazodone;
benzodiazepines are anticholinergic .
. non-sedating antipsychotics are also[6.29:
the most likely among
later generation antipsychotics to cause
akathisia (6.29:
that is the feeling of
getting sick from having to sit still;
but moving around doesn't really help
because the lack of stimulation
has to do with the way certain meds
can affect your neuro-hormones .
people with natural akathisia
are said to have attention deficit disorder,
and the cure is amphetamines;
generally the opposite of anti-dopaminergics)
. akathisia is more likely in
the higher-powered 1st-gen's
(they have less anticholinergic properties);
so they may be co.used with
sedatives:
# beta-adrenergic blockers
(propranolol or nadolol);
# or rarely a benzodiazepine or clonidine .
. quetiapine induces cataracts in animals
so the product label susggests slit-lamp exam's;
ophthalmologic studies find no evidence
supporting regular eye exam's;
however, since schiz'ics have
other risk factors for cataracts,
a referral to an ophthalmologist
for an eye exam
can be part of routine medical care
. diabetic ketoacidosis remains a rare possiblity[ziprasidone is not a sedative;
for all these antipsychotics .
. among the new anti-aggressives,
ziprasidone and aripiprazole cause
the least weight gain,
. all schiz'ics on 2nd-generation antipsychotics[is ziprasidone 2nd generation?
should be monitored at least twice yearly
for glucose abnormalities
and lipid profile .
. Se-MSC rapidly and specifically down-regulatesProgrammed Cell Death
expression of the Bcl-2 at transcriptional level.
The forced expression of Bcl-2
attenuated Se-MSC plus TRAIL-mediated apoptosis,
suggesting that Se-MSC's reduction of Bcl-2 expression
is critical to the increased sensitivity
to TRAIL in renal cancer cells.
In addition, we demonstrate that the synergistic effects
of Se-MSC and TRAIL
result from the activation of the
caspase-dependent pathways.
Co-administration of HA14-1,
a small molecule Bcl-2 inhibitor
and TRAIL increased apoptosis in Caki cells.
Taken together, Se-MSC-mediated down-regulation of Bcl-2
is able to sensitize Caki cells for
TRAIL-induced apoptosis.
Programmed cell death (PCD), or apoptosis,Se-methylselenocysteine inhibits
can be triggered by a wide range of stimuli,
including cell surface receptors like Fas
or tumor necrosis factor receptor 1 (TNFR1).
It constitutes a system for the removal of
unnecessary, aged, or damaged cells
. the relative abundance of
proapoptotic and antiapoptotic proteins
determines the susceptibility of the cell
to programmed death.
The proapoptotic proteins Bax, Bad, Bid, Bik, and Bim
contain an a-helical BH3 death domain
that fits the hydrophobic BH3 binding pocket
on the antiapoptotic proteins Bcl-2 and Bcl-xL,
forming heterodimers that block
the survival-promoting activity of Bcl-2 and Bcl-xL.
. things that result in more pro-apopt's
include: growth factor withdrawal
, genotoxic insult
, uv irradiation,
-- this reminds that chronically high
insulin (a growth factor)
can reduce one of your own sources of pro-apopt's .
The proapoptotic proteins act at
the surface of the mitochondrial membrane
to decrease the mitochondrial transmembrane potential
and promote leakage of cytochrome c.
In the presence of dATP,
cytochrome c complexes with and activates Apaf-1.
Activated Apaf-1 binds to downstream caspases,
such as pro-caspase-9,
and processes them into
proteolytically active forms.
This begins a caspase cascade
resulting in apoptosis.
Smac/Diablo is released from the mitochondria
and blocks IAP proteins that normally interact with
caspase-9 to inhibit its conversion to
the apoptosis-effecting caspases-{3, 6, 7}
The graphic shows the conserved apoptotic pathway
in the organism C. elegans .
CED-3 encodes a caspase whose function is facilitated by CED-4,
which is highly similar to Apaf-1.
CED-4 function is blocked by CED-9,
which protects cells against apoptosis
and is similar to the human antiapoptotic protein Bcl-2.
CED-9 activity is inhibited by EGL-1,
which is similar to the proapoptotic Bcl-2 family members.
Se-methylselenocysteine (MSC),Se-methylselenocysteine (MSC) chemically synthesized:
a naturally occurring selenium compound,
is a promising chemopreventive agent
against in vivo and in vitro models of
carcinogen-induced mouse and rat mammary tumorigenesis.
We have demonstrated previously that MSC
induces apoptosis after a cell growth arrest in S phase
in a mouse mammary epithelial tumor cell model (TM6 cells) in vitro.
The present study was designed to examine the involvement of
the phosphatidylinositol 3-kinase (PI3-K) pathway
in TM6 tumor model in vitro after treatment with MSC.
RESULTS: PI3-K activity was inhibited by MSC
followed by dephosphorylation of Akt.
The phosphorylation of p38 MAPK was also downregulated
after these cells were treated with MSC.
In parallel experiments MSC inhibited the
Raf-MEK-ERK signaling pathway.
CONCLUSION:
These studies suggest that MSC blocks
multiple signaling pathways
in mouse mammary tumor cells.
MSC inhibits cell growth by inhibiting the activity of PI3-K
and its downstream effector molecules
in mouse mammary tumor cells in vitro.
Methylated selenides are prominent metabolitesat the dietary levels-- Sodium selenite was obtained from
used for obtaining anticarcinogenic effects with selenium.
The present study reports the chemopreventive activities
of 2 novel selenium compounds,
Se-methylselenocysteine and
dimethyl selenoxide,
Other treatment groups were supplemented with either
selenite or selenocystine for comparative purposes.
Results of the carcinogenesis experiments showed that
the relative efficacy with the four compounds was
Se-methylselenocysteine > selenite
> selenocystine > dimethyl selenoxide.
In correlating the chemical form
and metabolism of these selenium compounds
with their anticarcinogenic activity,
it is concluded that:
(a) selenium compounds that are able to generate
a steady stream of methylated metabolites,
particularly the monomethylated species,
are likely to have good chemopreventive potential;
(b) anticarcinogenic activity is lower for selenoamino acids,
such as selenocysteine following conversion from selenocystine,
which have an escape mechanism via
random, nonstoichiometric incorporation into proteins;
(c) forms of selenium, as exemplified by
dimethyl selenoxide,
which are metabolized rapidly and quantitatively
to dimethyl selenide and trimethylselenonium
and excreted,
are likely to be poor choices.
We also undertook a separate bioavailability study
using
Se-methylselenocysteine
, dimethyl selenoxide
, and trimethylselenonium
as the starting compounds for delivering selenium with
one, two, or three methyl groups,
and measured the ability of these compounds to restore
glutathione peroxidase activity in selenium-depleted animals.
All three compounds were able to
fully replete this enzyme,
although with a wide range of efficiency
(Se-methylselenocysteine >
dimethyl selenoxide > trimethylselenonium),
suggesting that complete demethylation
to inorganic selenium
is a normal process of selenium metabolism.
However, the degree to which this occurs
under chemoprevention conditions
would argue against the involvement of selenoproteins
in the anticarcinogenic action of these selenium compounds.
CAS Number: 863394-07-4Sigma-Aldrich Corp
Empirical Formula (Hill Notation): C4H9NO2Se · HCl
Molecular Weight: 218.54
MDL number: MFCD03412450
PubChem Substance ID: 24278564
Description: Se-(Methyl)selenocysteine
. a chemopreventive agent that blocks
cell cycle progression and proliferation of
premalignant mammary lesions;
and, induces apoptosis of cancer cell lines in culture.
M6680-100MG /$ 164.50
# Opening a Sigma-Aldrich Account12.12: news.health/se/se-methylselenocysteine/Protease inhibitors:
Accounts are generally established for a company or institution
rather than for individuals.
# Your business or institution must have an established
Customer Account with Sigma-Aldrich
to establish an account, and be approved for on-line ordering;
you will need to contact Support by phone.
You cannot establish an account on-line.
These results confirm previous observations12.26: health/se/age-related macular degeneration:
that caspase-3 is crucial for inducing apoptosis by MSC treatment,
and further suggest the possibility that
an unknown member of the serine protease family
is involved in MSC-mediated apoptosis.
Our results strengthen the possibility that
MSC can be used to prevent or cure cancer
as either a chemopreventive or a chemotherapeutic agent.
Further studies are required to differentiate between
the chemopreventive effects on normal cells
and cancer cells in vitro.
CONCLUSIONS:12.26: web.health/se/macular degeneration/se's role:
On the basis of this preliminary open study
it seems that melatonin administration
may be beneficial for elderly subjects.
A significant decrease of estradiol concentrations
was observed after 6 months of the melatonin treatment
in comparison to initial levels.
IGF-I was found to be slightly but significantly
increased after the 6 months melatonin therapy.
Cortisol levels did not change significantly,
during the melatonin treatment.
DHEAS concentrations increased
after melatonin therapy.
-- a higher DHEAS/cortisol ratio .
Melatonin treatment did not influence significantly
either the parameters of total blood count
or glucose and serum lipids levels.
OBJECTIVES:
The role of melatonin in aging
is still under debate.
Therefore, an open pilot study on the effects of melatonin
was performed in elderly women.
SUBJECTS AND METHODS:
The study was performed on 14 women (volunteers),
aged from 64 to 80 years (mean age 71±4.6 years).
Melatonin (2 mg daily at 19:00 h) was administered during 6 months.
Before and after melatonin treatment
the peripheral venous blood samples
were taken in the morning (approx. at 08:00 h)
after the overnight fast.
The total blood count, glucose, total cholesterol,
LDL, HDL, and triglycerides were estimated by
routine laboratory methods.
The serum concentrations of the following hormones
were determined: 17-beta-estradiol,
dehydroepiandrosterone sulfate (DHEAS),
cortisol, and somatomedin C (IGF-I).
# Glutathione and its related enzyme precursor amino acids[. interesting term: diabetic macular edema
(N-Acetyl-Cysteine, L-glycine and glutamine,
as well as selenium)
are protective against damage to
human retinal pigment epithelium cells,
and may help prevent retinal damage in AMD.
Invest Ophthalmol Vis Sci 1993 Dec;34(13):3661-8
# Consumption of fruits and vegetables is protective against
progression of macular degeneration.
Cho, Seddon, et al Arch Ophthalmol. 2004 Jun;122(6):883-92
# In a clinical trial 60% of subjects with ARMD
or diabetic macular edema [...] So Med J, 1987.